Elevated AGE-Modified ApoB in Sera of Euglycemic, Normolipidemic Patients with Atherosclerosis: Relationship to Tissue AGEs

Stitt, Alan W.; He, Cijiang; Friedman, Steven G.; Scher, Larry A.; Rossi, P; Ong, Lydia; Founds, Hank; Li, Yong Ming; Bucala, Richard; Vlassara, Helen

doi:10.1007/bf03401819

Cited by 112 publications

(85 citation statements)

References 39 publications

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“…A positive correlation between circulating AGE-LDL, vascular tissue AGE, and lesion severity has been shown in nondiabetic patients with occlusive vascular disease (53). A rise in AGE-LDL due to impaired LDL-receptor clearance of LDL (14) would favor tissue AGE-lipid accumulation and inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy

Vlassara

Cai

Crandall

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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629

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Diet is a major environmental source of proinflammatory AGEs (heat-generated advanced glycation end products); its impact in humans remains unclear. We explored the effects of two equivalent diets, one regular (high AGE, H-AGE) and the other with 5-fold lower AGE (L-AGE) content on inflammatory mediators of 24 diabetic subjects: 11 in a 2-week crossover and 13 in a 6-week study. After 2 weeks on H-AGE, serum AGEs increased by 64.5% ( P = 0.02) and on L-AGE decreased by 30% ( P = 0.02). The mononuclear cell tumor necrosis factor-α/β-actin mRNA ratio was 1.4 ± 0.5 on H-AGE and 0.9 ± 0.5 on L-AGE ( P = 0.05), whereas serum vascular adhesion molecule-1 was 1,108 ± 429 and 698 ± 347 ng/ml ( P = 0.01) on L- and H-AGE, respectively. After 6 weeks, peripheral blood mononuclear cell tumor necrosis factor-α rose by 86.3% ( P = 0.006) and declined by 20% ( P , not significant) on H- or L-AGE diet, respectively; C-reactive protein increased by 35% on H-AGE and decreased by 20% on L-AGE ( P = 0.014), and vascular adhesion molecule-1 declined by 20% on L-AGE ( P < 0.01) and increased by 4% on H-AGE. Serum AGEs were increased by 28.2% on H-AGE ( P = 0.06) and reduced by 40% on L-AGE ( P = 0.02), whereas AGE low density lipoprotein was increased by 32% on H-AGE and reduced by 33% on L-AGE diet ( P < 0.05). Thus in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury. Restriction of dietary AGEs suppresses these effects.

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Section: Discussionmentioning

confidence: 99%

Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy

Vlassara

Cai

Crandall

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

629

530

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“…However, a reasonable choice for making valuable correlations possible was the measurement of CML, a common end product of glucoseprotein-and glucose-lipid-derived glycoxidative reactions, occurring abundantly in vivo and in heat-processed foods. 18,32 Also, CML-like AGE deposits are shown to correspond to the vascular pathology 33 and to the subinflammatory state of diabetes. 18 Of note, circulating CML also paralleled levels of ingested CML.…”

Section: Discussionmentioning

confidence: 97%

High Levels of Dietary Advanced Glycation End Products Transform Low-Dersity Lipoprotein Into a Potent Redox-Sensitive Mitogen-Activated Protein Kinase Stimulant in Diabetic Patients

et al. 2004

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Background-LDL modification by endogenous advanced glycation end products (AGEs) is thought to contribute to cardiovascular disease of diabetes. It remains unclear, however, whether exogenous (diet-derived) AGEs influence glycoxidation and endothelial cell toxicity of diabetic LDL. Methods and Results-Twenty-four diabetic subjects were randomized to either a standard diet (here called high-AGE, HAGE) or a diet 5-fold lower in AGE (LAGE diet) for 6 weeks. LDL pooled from patients on HAGE diet (Db-HAGE-LDL) was more glycated than LDL from the LAGE diet group (

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“…Glycated ApoB has been found in the macrophages of the arterial wall, in the fatty streaks of atherosclerotic vessels [36]. In fact, macrophages prefer glycated, oxidized or glyco-oxidized lipoproteins for their scavenger receptors, not the normal ones [34].…”

Section: Discussionmentioning

confidence: 99%

Nutrition, metabolism and colorectal cancer

Misciagna

Caruso

Trevisan³

2008

Genes Nutr

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Colorectal cancer and myocardial infarction are associated at population level and in autoptic studies. Furthermore, they share many blood variables: cholesterol, triglycerides and HDL cholesterol, fructosamine, glycated haemoglobin and glycated apolipoprotein B. These blood variables are intermediates between dietary, mainly saturated fats and high glycemic index and load diets, and colorectal cancer and myocardial infarction. Blood intermediate variables can be used in dietary trials as outcomes, and even to throw light on the pathogenesis of both diseases.

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Elevated AGE-Modified ApoB in Sera of Euglycemic, Normolipidemic Patients with Atherosclerosis: Relationship to Tissue AGEs

Cited by 112 publications

References 39 publications

Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy

Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy

High Levels of Dietary Advanced Glycation End Products Transform Low-Dersity Lipoprotein Into a Potent Redox-Sensitive Mitogen-Activated Protein Kinase Stimulant in Diabetic Patients

Nutrition, metabolism and colorectal cancer

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